Targeting a cell state common to triple‐negative breast cancers
Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple‐negative breast cancer (TNBC), no frequently recurring aberrations could be identified to make such an approach clinically feasible. Characterized by a highly heterogeneo...
Saved in:
| Published in | Molecular systems biology Vol. 11; no. 2; pp. 789 - n/a |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.02.2015
EMBO Press BlackWell Publishing Ltd Springer Nature |
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple‐negative breast cancer (TNBC), no frequently recurring aberrations could be identified to make such an approach clinically feasible. Characterized by a highly heterogeneous mutational landscape with few common features, many TNBCs cluster together based on their ‘basal‐like’ transcriptional profiles. We therefore hypothesized that targeting TNBC cells on a systems level by exploiting the transcriptional cell state might be a viable strategy to find novel therapies for this highly aggressive disease. We performed a large‐scale chemical genetic screen and identified a group of compounds related to the drug PKC412 (midostaurin). PKC412 induced apoptosis in a subset of TNBC cells enriched for the basal‐like subtype and inhibited tumor growth
in vivo
. We employed a multi‐omics approach and computational modeling to address the mechanism of action and identified spleen tyrosine kinase (SYK) as a novel and unexpected target in TNBC. Quantitative phosphoproteomics revealed that SYK inhibition abrogates signaling to STAT3, explaining the selectivity for basal‐like breast cancer cells. This non‐oncogene addiction suggests that chemical SYK inhibition may be beneficial for a specific subset of TNBC patients and demonstrates that targeting cell states could be a viable strategy to discover novel treatment strategies.
Synopsis
A chemical screen and systems approach reveal SYK‐STAT3 signaling as a druggable target in basal‐like breast cancers. The study supports the systems‐based notion that targeting a cell state, rather than a mutational state, can lead to therapeutic target discovery.
A chemical screen identifies a set of structurally related small molecules, including the drug midostaurin (PKC412), that target the mesenchymal cell state found in a subset of breast tumors.
A multi‐omics approach is combined with computational modeling for examining the drug mechanism of action and reveals the tyrosine kinase SYK as a novel breast cancer target.
Phospho‐proteomics analysis shows that SYK is required to maintain STAT3 phosphorylation in basal‐like breast cancer cells.
Graphical Abstract
A chemical screen and systems approach reveal SYK‐STAT3 signaling as a druggable target in basal‐like breast cancers. The study supports the systems‐based notion that targeting a cell state, rather than a mutational state, can lead to therapeutic target discovery. |
|---|---|
| AbstractList | Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple-negative breast cancer (TNBC), no frequently recurring aberrations could be identified to make such an approach clinically feasible. Characterized by a highly heterogeneous mutational landscape with few common features, many TNBCs cluster together based on their ‘basal-like’ transcriptional profiles. We therefore hypothesized that targeting TNBC cells on a systems level by exploiting the transcriptional cell state might be a viable strategy to find novel therapies for this highly aggressive disease. We performed a large-scale chemical genetic screen and identified a group of compounds related to the drug PKC412 (midostaurin). PKC412 induced apoptosis in a subset of TNBC cells enriched for the basal-like subtype and inhibited tumor growth in vivo. We employed a multi-omics approach and computational modeling to address the mechanism of action and identified spleen tyrosine kinase (SYK) as a novel and unexpected target in TNBC. Quantitative phosphoproteomics revealed that SYK inhibition abrogates signaling to STAT3, explaining the selectivity for basal-like breast cancer cells. This non-oncogene addiction suggests that chemical SYK inhibition may be beneficial for a specific subset of TNBC patients and demonstrates that targeting cell states could be a viable strategy to discover novel treatment strategies. Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple‐negative breast cancer (TNBC), no frequently recurring aberrations could be identified to make such an approach clinically feasible. Characterized by a highly heterogeneous mutational landscape with few common features, many TNBCs cluster together based on their ‘basal‐like’ transcriptional profiles. We therefore hypothesized that targeting TNBC cells on a systems level by exploiting the transcriptional cell state might be a viable strategy to find novel therapies for this highly aggressive disease. We performed a large‐scale chemical genetic screen and identified a group of compounds related to the drug PKC412 (midostaurin). PKC412 induced apoptosis in a subset of TNBC cells enriched for the basal‐like subtype and inhibited tumor growth in vivo. We employed a multi‐omics approach and computational modeling to address the mechanism of action and identified spleen tyrosine kinase (SYK) as a novel and unexpected target in TNBC. Quantitative phosphoproteomics revealed that SYK inhibition abrogates signaling to STAT3, explaining the selectivity for basal‐like breast cancer cells. This non‐oncogene addiction suggests that chemical SYK inhibition may be beneficial for a specific subset of TNBC patients and demonstrates that targeting cell states could be a viable strategy to discover novel treatment strategies. Synopsis A chemical screen and systems approach reveal SYK‐STAT3 signaling as a druggable target in basal‐like breast cancers. The study supports the systems‐based notion that targeting a cell state, rather than a mutational state, can lead to therapeutic target discovery. A chemical screen identifies a set of structurally related small molecules, including the drug midostaurin (PKC412), that target the mesenchymal cell state found in a subset of breast tumors. A multi‐omics approach is combined with computational modeling for examining the drug mechanism of action and reveals the tyrosine kinase SYK as a novel breast cancer target. Phospho‐proteomics analysis shows that SYK is required to maintain STAT3 phosphorylation in basal‐like breast cancer cells. A chemical screen and systems approach reveal SYK‐STAT3 signaling as a druggable target in basal‐like breast cancers. The study supports the systems‐based notion that targeting a cell state, rather than a mutational state, can lead to therapeutic target discovery. Abstract Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple‐negative breast cancer (TNBC), no frequently recurring aberrations could be identified to make such an approach clinically feasible. Characterized by a highly heterogeneous mutational landscape with few common features, many TNBCs cluster together based on their ‘basal‐like’ transcriptional profiles. We therefore hypothesized that targeting TNBC cells on a systems level by exploiting the transcriptional cell state might be a viable strategy to find novel therapies for this highly aggressive disease. We performed a large‐scale chemical genetic screen and identified a group of compounds related to the drug PKC412 (midostaurin). PKC412 induced apoptosis in a subset of TNBC cells enriched for the basal‐like subtype and inhibited tumor growth in vivo. We employed a multi‐omics approach and computational modeling to address the mechanism of action and identified spleen tyrosine kinase (SYK) as a novel and unexpected target in TNBC. Quantitative phosphoproteomics revealed that SYK inhibition abrogates signaling to STAT3, explaining the selectivity for basal‐like breast cancer cells. This non‐oncogene addiction suggests that chemical SYK inhibition may be beneficial for a specific subset of TNBC patients and demonstrates that targeting cell states could be a viable strategy to discover novel treatment strategies. Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple‐negative breast cancer (TNBC), no frequently recurring aberrations could be identified to make such an approach clinically feasible. Characterized by a highly heterogeneous mutational landscape with few common features, many TNBCs cluster together based on their ‘basal‐like’ transcriptional profiles. We therefore hypothesized that targeting TNBC cells on a systems level by exploiting the transcriptional cell state might be a viable strategy to find novel therapies for this highly aggressive disease. We performed a large‐scale chemical genetic screen and identified a group of compounds related to the drug PKC412 (midostaurin). PKC412 induced apoptosis in a subset of TNBC cells enriched for the basal‐like subtype and inhibited tumor growth in vivo . We employed a multi‐omics approach and computational modeling to address the mechanism of action and identified spleen tyrosine kinase (SYK) as a novel and unexpected target in TNBC. Quantitative phosphoproteomics revealed that SYK inhibition abrogates signaling to STAT3, explaining the selectivity for basal‐like breast cancer cells. This non‐oncogene addiction suggests that chemical SYK inhibition may be beneficial for a specific subset of TNBC patients and demonstrates that targeting cell states could be a viable strategy to discover novel treatment strategies. Synopsis A chemical screen and systems approach reveal SYK‐STAT3 signaling as a druggable target in basal‐like breast cancers. The study supports the systems‐based notion that targeting a cell state, rather than a mutational state, can lead to therapeutic target discovery. A chemical screen identifies a set of structurally related small molecules, including the drug midostaurin (PKC412), that target the mesenchymal cell state found in a subset of breast tumors. A multi‐omics approach is combined with computational modeling for examining the drug mechanism of action and reveals the tyrosine kinase SYK as a novel breast cancer target. Phospho‐proteomics analysis shows that SYK is required to maintain STAT3 phosphorylation in basal‐like breast cancer cells. Graphical Abstract A chemical screen and systems approach reveal SYK‐STAT3 signaling as a druggable target in basal‐like breast cancers. The study supports the systems‐based notion that targeting a cell state, rather than a mutational state, can lead to therapeutic target discovery. Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple-negative breast cancer (TNBC), no frequently recurring aberrations could be identified to make such an approach clinically feasible. Characterized by a highly heterogeneous mutational landscape with few common features, many TNBCs cluster together based on their 'basal-like' transcriptional profiles. We therefore hypothesized that targeting TNBC cells on a systems level by exploiting the transcriptional cell state might be a viable strategy to find novel therapies for this highly aggressive disease. We performed a large-scale chemical genetic screen and identified a group of compounds related to the drug PKC412 (midostaurin). PKC412 induced apoptosis in a subset of TNBC cells enriched for the basal-like subtype and inhibited tumor growth in vivo. We employed a multi-omics approach and computational modeling to address the mechanism of action and identified spleen tyrosine kinase (SYK) as a novel and unexpected target in TNBC. Quantitative phosphoproteomics revealed that SYK inhibition abrogates signaling to STAT3, explaining the selectivity for basal-like breast cancer cells. This non-oncogene addiction suggests that chemical SYK inhibition may be beneficial for a specific subset of TNBC patients and demonstrates that targeting cell states could be a viable strategy to discover novel treatment strategies.Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple-negative breast cancer (TNBC), no frequently recurring aberrations could be identified to make such an approach clinically feasible. Characterized by a highly heterogeneous mutational landscape with few common features, many TNBCs cluster together based on their 'basal-like' transcriptional profiles. We therefore hypothesized that targeting TNBC cells on a systems level by exploiting the transcriptional cell state might be a viable strategy to find novel therapies for this highly aggressive disease. We performed a large-scale chemical genetic screen and identified a group of compounds related to the drug PKC412 (midostaurin). PKC412 induced apoptosis in a subset of TNBC cells enriched for the basal-like subtype and inhibited tumor growth in vivo. We employed a multi-omics approach and computational modeling to address the mechanism of action and identified spleen tyrosine kinase (SYK) as a novel and unexpected target in TNBC. Quantitative phosphoproteomics revealed that SYK inhibition abrogates signaling to STAT3, explaining the selectivity for basal-like breast cancer cells. This non-oncogene addiction suggests that chemical SYK inhibition may be beneficial for a specific subset of TNBC patients and demonstrates that targeting cell states could be a viable strategy to discover novel treatment strategies. Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple-negative breast cancer (TNBC), no frequently recurring aberrations could be identified to make such an approach clinically feasible. Characterized by a highly heterogeneous mutational landscape with few common features, many TNBCs cluster together based on their ‘basal-like’ transcriptional profiles. We therefore hypothesized that targeting TNBC cells on a systems level by exploiting the transcriptional cell state might be a viable strategy to find novel therapies for this highly aggressive disease. We performed a large-scale chemical genetic screen and identified a group of compounds related to the drug PKC412 (midostaurin). PKC412 induced apoptosis in a subset of TNBC cells enriched for the basal-like subtype and inhibited tumor growth in vivo . We employed a multi-omics approach and computational modeling to address the mechanism of action and identified spleen tyrosine kinase (SYK) as a novel and unexpected target in TNBC. Quantitative phosphoproteomics revealed that SYK inhibition abrogates signaling to STAT3, explaining the selectivity for basal-like breast cancer cells. This non-oncogene addiction suggests that chemical SYK inhibition may be beneficial for a specific subset of TNBC patients and demonstrates that targeting cell states could be a viable strategy to discover novel treatment strategies. |
| Author | Lechtermann, Hannelore Trefzer, Claudia Serra, Violeta Leitner, Ernestine Kubicek, Stefan Müller, André C Kerzendorfer, Claudia Mair, Barbara Macho‐Maschler, Sabine Ibrahim, Yasir Klepsch, Freya Colinge, Jacques Nijman, Sebastian MB Baselga, José Muellner, Markus K Superti‐Furga, Giulio Bennett, Keiryn L Rix, Uwe |
| Author_xml | – sequence: 1 givenname: Markus K surname: Muellner fullname: Muellner, Markus K organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 2 givenname: Barbara surname: Mair fullname: Mair, Barbara organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 3 givenname: Yasir surname: Ibrahim fullname: Ibrahim, Yasir organization: Experimental Therapeutics Group, Vall d'Hebron Institute of Oncology – sequence: 4 givenname: Claudia surname: Kerzendorfer fullname: Kerzendorfer, Claudia organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 5 givenname: Hannelore surname: Lechtermann fullname: Lechtermann, Hannelore organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 6 givenname: Claudia surname: Trefzer fullname: Trefzer, Claudia organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 7 givenname: Freya surname: Klepsch fullname: Klepsch, Freya organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 8 givenname: André C surname: Müller fullname: Müller, André C organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 9 givenname: Ernestine surname: Leitner fullname: Leitner, Ernestine organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 10 givenname: Sabine surname: Macho‐Maschler fullname: Macho‐Maschler, Sabine organization: University of Veterinary Medicine – sequence: 11 givenname: Giulio orcidid: 0000-0002-0570-1768 surname: Superti‐Furga fullname: Superti‐Furga, Giulio organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 12 givenname: Keiryn L surname: Bennett fullname: Bennett, Keiryn L organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 13 givenname: José surname: Baselga fullname: Baselga, José organization: Memorial Sloan‐Kettering Cancer Center – sequence: 14 givenname: Uwe surname: Rix fullname: Rix, Uwe organization: H. Lee Moffitt Cancer Center and Research Institute – sequence: 15 givenname: Stefan surname: Kubicek fullname: Kubicek, Stefan organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 16 givenname: Jacques surname: Colinge fullname: Colinge, Jacques organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences – sequence: 17 givenname: Violeta surname: Serra fullname: Serra, Violeta organization: Experimental Therapeutics Group, Vall d'Hebron Institute of Oncology – sequence: 18 givenname: Sebastian MB surname: Nijman fullname: Nijman, Sebastian MB email: snijman@cemm.oeaw.ac.at organization: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25699542$$D View this record in MEDLINE/PubMed https://hal.umontpellier.fr/hal-02276743$$DView record in HAL |
| BookMark | eNp9kstu1DAUhiNURC-wZIsisYFFBt8Tb5CGqtBKg1hQ1pbtnKQeJfZgZwZ1xyP0GXkSMk2ntCNgZev4-__jcznODnzwkGUvMZphTjh51yczIwgzLgR7kh3hkrGCEUkOHtwPs-OUlgjRClfkWXZIuJCSM3KUzS91bGFwvs11bqHr8jToAXIb-j74fAj5EN2qg18_bzy0enAbyE0EnYbcam8hpufZ00Z3CV7cnSfZt49nl6fnxeLLp4vT-aKwgpSs0I3hNSPcEt4IbkCWGhPKLegSDAJmSqQrYSiYGvHGEkLqSkuMKouZpkzQk-xi8q2DXqpVdL2O1ypop24DIbZKx8HZDhSirJHGNIaSmhlZGlFJy22DrKxw02y93k9eq7Xpobbgh6i7R6aPX7y7Um3YKEZ5JQQaDd5OBld7svP5Qm1jiJBSlIxu8Mi-uUsWw_c1pEH1Lm1brT2EdVJY8JKSipZ0RF_vocuwjn5sqyJEIiw54mykXj38_X3-3VRHgE6AjSGlCI2ybpyqC9tiXKcwUre7o8bdUbvdGVXFnmpn_C-eTfwP18H1_2H1-euHe9lskqVR4VuIf2r8e57fRnLkFA |
| CitedBy_id | crossref_primary_10_1186_s12943_016_0515_5 crossref_primary_10_1186_s12943_016_0517_3 crossref_primary_10_18632_oncotarget_24853 crossref_primary_10_1016_j_ejmech_2015_07_034 crossref_primary_10_1080_14789450_2024_2432477 crossref_primary_10_3390_cancers14071603 crossref_primary_10_1016_j_pharmthera_2016_11_011 crossref_primary_10_1016_j_tips_2015_08_009 crossref_primary_10_1016_j_trac_2022_116862 crossref_primary_10_1016_j_compbiolchem_2024_108154 crossref_primary_10_1002_ptr_6189 crossref_primary_10_1016_j_semcancer_2020_02_003 crossref_primary_10_1002_pmic_201600235 crossref_primary_10_1002_1878_0261_12202 crossref_primary_10_1042_BCJ20160782 crossref_primary_10_3389_fonc_2019_01408 crossref_primary_10_1111_febs_16442 crossref_primary_10_1038_s41388_017_0113_z crossref_primary_10_2217_pme_2016_0020 |
| Cites_doi | 10.1016/j.ccr.2006.10.008 10.1038/onc.2009.99 10.1186/bcr1982 10.1371/journal.pone.0007445 10.1200/JCO.2001.19.5.1485 10.1038/sj.onc.1204349 10.1093/annonc/mds586 10.3322/caac.20107 10.1093/annonc/mdh052 10.1371/journal.pcbi.1001001 10.1021/ci100031x 10.1038/nrclinonc.2010.154 10.1016/S0022-2836(77)80200-3 10.1158/1078-0432.CCR-08-1155 10.1158/1078-0432.CCR-06-3045 10.1186/bcr2635 10.1038/nchembio.216 10.1158/1535-7163.MCT-12-0441-T 10.1021/ac802720e 10.1200/JCO.2006.06.5664 10.1074/jbc.M409792200 10.1126/science.89.2312.365-a 10.1158/1078-0432.CCR-12-1611 10.1158/2159-8290.CD-11-0348 10.1021/ci700052x 10.1593/neo.91084 10.1186/bcr2108 10.1016/S0092-8674(00)81959-5 10.1021/ci300314k 10.1038/nature11412 10.1016/j.cell.2007.09.007 10.1038/nature10983 10.1200/JCO.2010.28.9678 10.1098/rstb.2011.0008 10.1182/blood-2009-08-236471 10.1016/j.ajhg.2008.02.013 10.1210/en.2002-220224 10.1073/pnas.0810772105 10.1101/gad.10.19.2462 10.1101/gad.13.19.2604 10.1158/1541-7786.MCR-08-0371 10.1038/nm.2454 10.1172/JCI44745 10.1016/S0167-5699(99)01574-1 10.1021/jm00084a004 10.1056/NEJMoa063994 10.1158/0008-5472.CAN-08-3441 10.1038/35021093 10.1038/onc.2013.185 10.1002/prca.201100077 10.1038/35021086 |
| ContentType | Journal Article |
| Copyright | The Author(s) 2015 2015 The Authors. Published under the terms of the CC BY 4.0 license 2015 The Authors. Published under the terms of the CC BY 4.0 license. 2015. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Attribution 2015 The Authors. Published under the terms of the CC BY 4.0 license 2015 |
| Copyright_xml | – notice: The Author(s) 2015 – notice: 2015 The Authors. Published under the terms of the CC BY 4.0 license – notice: 2015 The Authors. Published under the terms of the CC BY 4.0 license. – notice: 2015. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: Attribution – notice: 2015 The Authors. Published under the terms of the CC BY 4.0 license 2015 |
| DBID | C6C 24P AAYXX CITATION CGR CUY CVF ECM EIF NPM 3V. 7QL 7TM 7U9 7X7 7XB 88A 88E 8AO 8FD 8FE 8FH 8FI 8FJ 8FK 8G5 ABUWG AEUYN AFKRA AZQEC BBNVY BENPR BHPHI C1K CCPQU DWQXO FR3 FYUFA GHDGH GNUQQ GUQSH H94 HCIFZ K9. LK8 M0S M1P M2O M7N M7P MBDVC P64 PADUT PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PRINS Q9U RC3 7X8 1XC VOOES 5PM DOA |
| DOI | 10.15252/msb.20145664 |
| DatabaseName | Springer Nature OA Free Journals Wiley Online Library Open Access CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Central (Corporate) Bacteriology Abstracts (Microbiology B) Nucleic Acids Abstracts Virology and AIDS Abstracts Health & Medical Collection ProQuest Central (purchase pre-March 2016) Biology Database (Alumni Edition) Medical Database (Alumni Edition) ProQuest Pharma Collection Technology Research Database ProQuest SciTech Collection ProQuest Natural Science Journals ProQuest Hospital Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) Research Library (Alumni) ProQuest Central (Alumni) ProQuest One Sustainability ProQuest Central UK/Ireland ProQuest Central Essentials - QC Biological Science Collection ProQuest Central Natural Science Collection Environmental Sciences and Pollution Management ProQuest One Community College ProQuest Central Engineering Research Database Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student ProQuest Research Library AIDS and Cancer Research Abstracts SciTech Premium Collection ProQuest Health & Medical Complete (Alumni) Biological Sciences ProQuest Health & Medical Collection Medical Database Research Library Algology Mycology and Protozoology Abstracts (Microbiology C) Biological Science Database Research Library (Corporate) Biotechnology and BioEngineering Abstracts Research Library China ProQuest Central Premium ProQuest One Academic (New) Publicly Available Content Database ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China ProQuest Central Basic Genetics Abstracts MEDLINE - Academic Hyper Article en Ligne (HAL) Hyper Article en Ligne (HAL) (Open Access) PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Publicly Available Content Database Research Library Prep ProQuest Central Student ProQuest Central Essentials Nucleic Acids Abstracts SciTech Premium Collection ProQuest Central China Environmental Sciences and Pollution Management ProQuest One Applied & Life Sciences ProQuest One Sustainability Health Research Premium Collection Natural Science Collection Health & Medical Research Collection Biological Science Collection ProQuest Central (New) Research Library China ProQuest Medical Library (Alumni) Virology and AIDS Abstracts ProQuest Biological Science Collection ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) Biological Science Database ProQuest Hospital Collection (Alumni) Biotechnology and BioEngineering Abstracts ProQuest Health & Medical Complete ProQuest One Academic UKI Edition Engineering Research Database ProQuest One Academic ProQuest One Academic (New) Technology Research Database ProQuest One Academic Middle East (New) ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest One Health & Nursing Research Library (Alumni Edition) ProQuest Natural Science Collection ProQuest Pharma Collection ProQuest Biology Journals (Alumni Edition) ProQuest Central ProQuest Health & Medical Research Collection Genetics Abstracts Health and Medicine Complete (Alumni Edition) ProQuest Central Korea Bacteriology Abstracts (Microbiology B) Algology Mycology and Protozoology Abstracts (Microbiology C) AIDS and Cancer Research Abstracts ProQuest Research Library ProQuest Central Basic ProQuest SciTech Collection ProQuest Medical Library ProQuest Central (Alumni) MEDLINE - Academic |
| DatabaseTitleList | Publicly Available Content Database MEDLINE MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: C6C name: Springer Nature OA Free Journals url: http://www.springeropen.com/ sourceTypes: Publisher – sequence: 2 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 3 dbid: 24P name: Wiley Open Access Collection url: https://authorservices.wiley.com/open-science/open-access/browse-journals.html sourceTypes: Publisher – sequence: 4 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 5 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 6 dbid: BENPR name: ProQuest Central url: https://www.proquest.com/central sourceTypes: Aggregation Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 1744-4292 |
| EndPage | n/a |
| ExternalDocumentID | oai_doaj_org_article_034f9bbfb32d4b97b689c5cf0c981ff6 PMC4358660 oai_HAL_hal_02276743v1 25699542 10_15252_msb_20145664 MSB145664 |
| Genre | article Research Support, Non-U.S. Gov't Journal Article |
| GrantInformation_xml | – fundername: Vienna Science and Technology Fund (WWTF) grantid: LS09‐009 – fundername: Austrian Science Fund (FWF) grantid: P21768‐B13; SFB‐F47 – fundername: Austrian Federal Ministry for Science and Research (BMWF) under the GEN‐AU program grantid: GZ 200.142/1‐VI/I/2006; GZ BMWF‐70.081/0018‐II/1a/2008) – fundername: ERC Starting grant grantid: 311166‐Gene.Drugs.Cancer – fundername: ERC Starting grant funderid: 311166‐Gene.Drugs.Cancer – fundername: Austrian Federal Ministry for Science and Research (BMWF) under the GEN‐AU program funderid: GZ 200.142/1‐VI/I/2006; GZ BMWF‐70.081/0018‐II/1a/2008) – fundername: Vienna Science and Technology Fund (WWTF) funderid: LS09‐009 – fundername: Austrian Science Fund (FWF) funderid: P21768‐B13; SFB‐F47 |
| GroupedDBID | --- -Q- 0R~ 123 1OC 24P 29M 2WC 39C 53G 5VS 7X7 88E 8AO 8FE 8FH 8FI 8FJ 8G5 8R4 8R5 AAJSJ AAMMB ABDBF ABUWG ACCMX ACGFO ACPRK ACUHS ACXQS ADBBV ADKYN ADRAZ ADZMN AEFGJ AEGXH AENEX AEUYN AFKRA AFRAH AGXDD AHMBA AIAGR AIDQK AIDYY ALIPV ALMA_UNASSIGNED_HOLDINGS ALUQN AOIJS AVUZU AZFZN AZQEC BAWUL BBNVY BCNDV BENPR BHPHI BPHCQ BVXVI C6C CAG CCPQU CS3 DIK DU5 DWQXO E3Z EBD EBS EJD EMB EMOBN ESX F5P FYUFA GNUQQ GROUPED_DOAJ GUQSH GX1 H13 HCIFZ HH5 HK~ HMCUK HYE HZ~ IAO IHR INH ITC KQ8 LK8 M1P M2O M48 M7P ML0 M~E NAO O5R O5S O9- OK1 OVT P2P PADUT PHGZM PHGZT PIMPY PJZUB PPXIY PQGLB PQQKQ PROAC PSQYO Q2X RHI RNS RNTTT RPM SV3 TR2 TUS UKHRP WIN WOQ WOW XSB ~8M 3V. 4.4 88A AAHHS ACCFJ AEEZP AEQDE AIWBW AJBDE COF EBLON GODZA IGS M0L AASML AAYXX CITATION CGR CUY CVF ECM EIF NPM 7QL 7TM 7U9 7XB 8FD 8FK C1K FR3 H94 K9. M7N MBDVC P64 PKEHL PQEST PQUKI PRINS Q9U RC3 7X8 1XC VOOES 5PM PUEGO |
| ID | FETCH-LOGICAL-c6274-afb5d425c25f65be97a1235cea7eb0e4b70a86b3ebd05fc222d8a9108c14a3463 |
| IEDL.DBID | M48 |
| ISSN | 1744-4292 |
| IngestDate | Wed Aug 27 01:29:34 EDT 2025 Thu Aug 21 13:49:42 EDT 2025 Fri May 09 12:17:19 EDT 2025 Thu Jul 10 17:43:12 EDT 2025 Wed Aug 13 08:49:12 EDT 2025 Mon Jul 21 05:58:59 EDT 2025 Tue Jul 01 04:10:33 EDT 2025 Thu Apr 24 22:53:49 EDT 2025 Wed Jan 22 16:41:58 EST 2025 Tue Aug 12 01:10:41 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 2 |
| Keywords | breast cancer small‐molecule screen cell state small-molecule screen |
| Language | English |
| License | Attribution http://creativecommons.org/licenses/by/4.0 2015 The Authors. Published under the terms of the CC BY 4.0 license. Attribution: http://creativecommons.org/licenses/by This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c6274-afb5d425c25f65be97a1235cea7eb0e4b70a86b3ebd05fc222d8a9108c14a3463 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 PMCID: PMC4358660 Subject Categories Genome-Scale & Integrative Biology; Pharmacology & Drug Discovery; Cancer |
| ORCID | 0000-0002-0570-1768 0000-0003-2466-4824 |
| OpenAccessLink | https://doaj.org/article/034f9bbfb32d4b97b689c5cf0c981ff6 |
| PMID | 25699542 |
| PQID | 2290195054 |
| PQPubID | 29031 |
| PageCount | 16 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_034f9bbfb32d4b97b689c5cf0c981ff6 pubmedcentral_primary_oai_pubmedcentral_nih_gov_4358660 hal_primary_oai_HAL_hal_02276743v1 proquest_miscellaneous_1657328373 proquest_journals_2290195054 pubmed_primary_25699542 crossref_citationtrail_10_15252_msb_20145664 crossref_primary_10_15252_msb_20145664 wiley_primary_10_15252_msb_20145664_MSB145664 springer_journals_10_15252_msb_20145664 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | February 2015 |
| PublicationDateYYYYMMDD | 2015-02-01 |
| PublicationDate_xml | – month: 02 year: 2015 text: February 2015 |
| PublicationDecade | 2010 |
| PublicationPlace | London |
| PublicationPlace_xml | – name: London – name: England – name: Oxford, UK |
| PublicationTitle | Molecular systems biology |
| PublicationTitleAbbrev | Mol Syst Biol |
| PublicationTitleAlternate | Mol Syst Biol |
| PublicationYear | 2015 |
| Publisher | Nature Publishing Group UK EMBO Press BlackWell Publishing Ltd Springer Nature |
| Publisher_xml | – name: Nature Publishing Group UK – name: EMBO Press – name: BlackWell Publishing Ltd – name: Springer Nature |
| References | 2010; 12 2012; 486 2009; 81 2011; 61 2008; 105 2011; 17 2012; 11 2012; 52 2013; 19 2010; 23 2009; 11 2011; 366 2006; 24 2002; 143 2010; 28 2010; 115 2007; 130 2000; 406 2003; 9 2012; 490 1999; 13 2001; 19 1999; 98 1939; 89 2010; 3 2012; 23 2010; 7 2010; 6 2009; 15 2011; 121 2009; 69 2006; 10 2000; 21 2002; 8 1992; 35 2008; 10 2007; 13 1996; 10 2001; 20 2009; 28 2007; 356 2012; 2 2004; 279 2004; 15 2009; 7 2009; 5 2009; 4 2012; 6 1977; 112 2008; 82 2014; 33 2007; 47 2010; 50 e_1_2_8_28_1 e_1_2_8_24_1 e_1_2_8_47_1 e_1_2_8_26_1 e_1_2_8_49_1 Armanious H (e_1_2_8_2_1) 2010; 3 Buettner R (e_1_2_8_8_1) 2002; 8 e_1_2_8_3_1 e_1_2_8_5_1 e_1_2_8_7_1 e_1_2_8_9_1 e_1_2_8_43_1 e_1_2_8_22_1 e_1_2_8_45_1 e_1_2_8_41_1 e_1_2_8_17_1 e_1_2_8_19_1 e_1_2_8_13_1 e_1_2_8_36_1 e_1_2_8_15_1 e_1_2_8_38_1 e_1_2_8_32_1 e_1_2_8_55_1 e_1_2_8_11_1 e_1_2_8_34_1 e_1_2_8_53_1 e_1_2_8_30_1 Dolled‐Filhart M (e_1_2_8_20_1) 2003; 9 e_1_2_8_29_1 e_1_2_8_25_1 e_1_2_8_46_1 e_1_2_8_27_1 e_1_2_8_48_1 Staff S (e_1_2_8_51_1) 2010; 23 e_1_2_8_4_1 e_1_2_8_6_1 e_1_2_8_21_1 e_1_2_8_42_1 e_1_2_8_23_1 e_1_2_8_44_1 e_1_2_8_40_1 e_1_2_8_18_1 e_1_2_8_39_1 e_1_2_8_14_1 e_1_2_8_35_1 e_1_2_8_16_1 e_1_2_8_37_1 e_1_2_8_10_1 e_1_2_8_31_1 e_1_2_8_56_1 e_1_2_8_12_1 e_1_2_8_33_1 e_1_2_8_54_1 e_1_2_8_52_1 e_1_2_8_50_1 21727130 - Philos Trans R Soc Lond B Biol Sci. 2011 Aug 12;366(1575):2247-59 875032 - J Mol Biol. 1977 May 25;112(3):535-42 17157791 - Cancer Cell. 2006 Dec;10(6):515-27 11948098 - Clin Cancer Res. 2002 Apr;8(4):945-54 19829710 - PLoS One. 2009;4(10):e7445 17116942 - J Clin Oncol. 2006 Dec 20;24(36):5652-7 19690537 - Nat Chem Biol. 2009 Sep;5(9):616-24 11230495 - J Clin Oncol. 2001 Mar 1;19(5):1485-92 20733134 - J Clin Oncol. 2010 Oct 1;28(28):4339-45 22522925 - Nature. 2012 Jun 21;486(7403):346-52 20235588 - J Chem Inf Model. 2010 Apr 26;50(4):572-84 20813035 - Breast Cancer Res. 2010;12(5):R68 17833344 - Science. 1939 Apr 21;89(2312):365-6 12193580 - Endocrinology. 2002 Sep;143(9):3641-50 23012245 - Mol Cancer Ther. 2012 Dec;11(12):2693-703 21633165 - J Clin Invest. 2011 Jul;121(7):2723-35 17889643 - Cell. 2007 Sep 21;130(6):986-8 18366788 - Breast Cancer Res. 2008;10(2):R25 20019840 - Neoplasia. 2009 Dec;11(12):1318-28 20043089 - Oncol Rep. 2010 Feb;23(2):307-12 17591764 - J Chem Inf Model. 2007 Jul-Aug;47(4):1504-19 19421152 - Oncogene. 2009 Jun 18;28(24):2337-47 20877296 - Nat Rev Clin Oncol. 2010 Dec;7(12):683-92 19331382 - Anal Chem. 2009 May 1;81(9):3440-7 12576423 - Clin Cancer Res. 2003 Feb;9(2):594-600 22213655 - Proteomics Clin Appl. 2012 Jan;6(1-2):102-16 15507431 - J Biol Chem. 2004 Dec 31;279(53):55827-32 17671126 - Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4429-34 19118038 - Clin Cancer Res. 2009 Jan 1;15(1):110-8 10963601 - Nature. 2000 Aug 17;406(6797):742-7 18559090 - Breast Cancer Res. 2008;10(3):R53 20830236 - Int J Clin Exp Pathol. 2010;3(7):654-64 21296855 - CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 19435916 - Cancer Res. 2009 May 15;69(10):4116-24 19965662 - Blood. 2010 Apr 1;115(13):2578-85 8843198 - Genes Dev. 1996 Oct 1;10(19):2462-77 10521404 - Genes Dev. 1999 Oct 1;13(19):2604-16 1552513 - J Med Chem. 1992 Mar 20;35(6):994-1001 22915752 - Cancer Discov. 2012 Nov;2(11):1036-47 11420660 - Oncogene. 2001 May 3;20(20):2499-513 18371930 - Am J Hum Genet. 2008 Apr;82(4):949-58 14760128 - Ann Oncol. 2004 Feb;15(2):316-23 22019887 - Nat Med. 2011;17(11):1514-20 23136197 - Clin Cancer Res. 2013 Jan 1;19(1):291-303 23728343 - Oncogene. 2014 May 8;33(19):2531-9 21124949 - PLoS Comput Biol. 2010;6(11):e1001001 10689303 - Immunol Today. 2000 Mar;21(3):148-54 10458605 - Cell. 1999 Aug 6;98(3):295-303 23166150 - Ann Oncol. 2012 Dec;23(12):2997-3006 19104045 - Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20870-5 23000897 - Nature. 2012 Oct 4;490(7418):61-70 17229949 - N Engl J Med. 2007 Jan 18;356(3):217-26 10963602 - Nature. 2000 Aug 17;406(6797):747-52 19435818 - Mol Cancer Res. 2009 May;7(5):634-44 23082786 - J Chem Inf Model. 2012 Nov 26;52(11):2919-36 |
| References_xml | – volume: 21 start-page: 148 year: 2000 end-page: 154 article-title: Tyrosine kinase SYK: essential functions for immunoreceptor signalling publication-title: Immunol Today – volume: 112 start-page: 535 year: 1977 end-page: 542 article-title: The Protein Data Bank: a computer‐based archival file for macromolecular structures publication-title: J Mol Biol – volume: 82 start-page: 949 year: 2008 end-page: 958 article-title: Walking the interactome for prioritization of candidate disease genes publication-title: Am J Hum Genet – volume: 24 start-page: 5652 year: 2006 end-page: 5657 article-title: Locoregional relapse and distant metastasis in conservatively managed triple negative early‐stage breast cancer publication-title: J Clin Oncol – volume: 6 start-page: 102 year: 2012 end-page: 116 article-title: Systems biology analysis of protein‐drug interactions publication-title: Proteomics Clin Appl – volume: 9 start-page: 594 year: 2003 end-page: 600 article-title: Tissue microarray analysis of signal transducers and activators of transcription 3 (Stat3) and phospho‐Stat3 (Tyr705) in node‐negative breast cancer shows nuclear localization is associated with a better prognosis publication-title: Clin Cancer Res – volume: 130 start-page: 986 year: 2007 end-page: 988 article-title: Non‐oncogene addiction and the stress phenotype of cancer cells publication-title: Cell – volume: 7 start-page: 683 year: 2010 end-page: 692 article-title: Triple‐negative breast cancer: disease entity or title of convenience? publication-title: Nat Rev Clin Oncol – volume: 13 start-page: 4429 year: 2007 end-page: 4434 article-title: Triple‐negative breast cancer: clinical features and patterns of recurrence publication-title: Clin Cancer Res – volume: 406 start-page: 747 year: 2000 end-page: 752 article-title: Molecular portraits of human breast tumours publication-title: Nature – volume: 115 start-page: 2578 year: 2010 end-page: 2585 article-title: Inhibition of Syk with fostamatinib disodium has significant clinical activity in non‐Hodgkin lymphoma and chronic lymphocytic leukemia publication-title: Blood – volume: 356 start-page: 217 year: 2007 end-page: 226 article-title: The prognostic role of a gene signature from tumorigenic breast‐cancer cells publication-title: N Engl J Med – volume: 61 start-page: 69 year: 2011 end-page: 90 article-title: Global cancer statistics publication-title: CA Cancer J Clin – volume: 4 start-page: e7445 year: 2009 article-title: Tumor suppressor function of Syk in human MCF10A in vitro and normal mouse mammary epithelium in vivo publication-title: PLoS One – volume: 15 start-page: 316 year: 2004 end-page: 323 article-title: Phase I study of PKC412 (N‐benzoyl‐staurosporine), a novel oral protein kinase C inhibitor, combined with gemcitabine and cisplatin in patients with non‐small‐cell lung cancer publication-title: Ann Oncol – volume: 19 start-page: 1485 year: 2001 end-page: 1492 article-title: Phase I and pharmacokinetic study of PKC412, an inhibitor of protein kinase C publication-title: J Clin Oncol – volume: 11 start-page: 2693 year: 2012 end-page: 2703 article-title: Inhibiting aurora kinases reduces tumor growth and suppresses tumor recurrence after chemotherapy in patient‐derived triple‐negative breast cancer xenografts publication-title: Mol Cancer Ther – volume: 20 start-page: 2499 year: 2001 end-page: 2513 article-title: Constitutive activation of Stat3 by the Src and JAK tyrosine kinases participates in growth regulation of human breast carcinoma cells publication-title: Oncogene – volume: 19 start-page: 291 year: 2013 end-page: 303 article-title: Predictive Biomarkers of Sensitivity to the Aurora and Angiogenic Kinase Inhibitor ENMD‐2076 in Preclinical Breast Cancer Models publication-title: Clin Cancer Res – volume: 5 start-page: 616 year: 2009 end-page: 624 article-title: Target profiling of small molecules by chemical proteomics publication-title: Nat Chem Biol – volume: 2 start-page: 1036 year: 2012 end-page: 1047 article-title: PI3K inhibition impairs BRCA1/2 expression and sensitizes BRCA‐proficient triple‐negative breast cancer to PARP inhibition publication-title: Cancer Discov – volume: 11 start-page: 1318 year: 2009 end-page: 1328 article-title: Twist modulates breast cancer stem cells by transcriptional regulation of CD24 expression publication-title: Neoplasia – volume: 81 start-page: 3440 year: 2009 end-page: 3447 article-title: Improved electrospray ionization efficiency compensates for diminished chromatographic resolution and enables proteomics analysis of tyrosine signaling in embryonic stem cells publication-title: Anal Chem – volume: 15 start-page: 110 year: 2009 end-page: 118 article-title: Broad antitumor activity in breast cancer xenografts by motesanib, a highly selective, oral inhibitor of vascular endothelial growth factor, platelet‐derived growth factor, and Kit receptors publication-title: Clin Cancer Res – volume: 47 start-page: 1504 year: 2007 end-page: 1519 article-title: Comparison of topological, shape, and docking methods in virtual screening publication-title: J Chem Inf Model – volume: 23 start-page: 2997 year: 2012 end-page: 3006 article-title: Molecular subclasses of breast cancer: how do we define them? The IMPAKT 2012 Working Group Statement publication-title: Ann Oncol – volume: 10 start-page: 2462 year: 1996 end-page: 2477 article-title: TGF‐beta1 and Ha‐Ras collaborate in modulating the phenotypic plasticity and invasiveness of epithelial tumor cells publication-title: Genes Dev – volume: 28 start-page: 2337 year: 2009 end-page: 2347 article-title: Phosphoproteomic analysis of Syk kinase signaling in human cancer cells reveals its role in cell‐cell adhesion publication-title: Oncogene – volume: 17 start-page: 1514 year: 2011 end-page: 1520 article-title: Tumor grafts derived from women with breast cancer authentically reflect tumor pathology, growth, metastasis and disease outcomes publication-title: Nat Med – volume: 23 start-page: 307 year: 2010 end-page: 312 article-title: Aurora‐A gene is frequently amplified in basal‐like breast cancer publication-title: Oncol Rep – volume: 89 start-page: 365 year: 1939 end-page: 366 article-title: Early man in western and northwestern Canada publication-title: Science – volume: 69 start-page: 4116 year: 2009 end-page: 4124 article-title: Characterization of a naturally occurring breast cancer subset enriched in epithelial‐to‐mesenchymal transition and stem cell characteristics publication-title: Cancer Res – volume: 366 start-page: 2247 year: 2011 end-page: 2259 article-title: Systems biology of stem cells: three useful perspectives to help overcome the paradigm of linear pathways publication-title: Philos Trans R Soc Lond B Biol Sci – volume: 143 start-page: 3641 year: 2002 end-page: 3650 article-title: Deletion of Stat3 blocks mammary gland involution and extends functional competence of the secretory epithelium in the absence of lactogenic stimuli publication-title: Endocrinology – volume: 10 start-page: 515 year: 2006 end-page: 527 article-title: A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes publication-title: Cancer Cell – volume: 279 start-page: 55827 year: 2004 end-page: 55832 article-title: A novel mode of Gleevec binding is revealed by the structure of spleen tyrosine kinase publication-title: J Biol Chem – volume: 121 start-page: 2723 year: 2011 end-page: 2735 article-title: The JAK2/STAT3 signaling pathway is required for growth of CD44(+)CD24(‐) stem cell‐like breast cancer cells in human tumors publication-title: J Clin Invest – volume: 12 start-page: R68 year: 2010 article-title: Phenotypic and molecular characterization of the claudin‐low intrinsic subtype of breast cancer publication-title: Breast Cancer Res – volume: 33 start-page: 2531 year: 2014 end-page: 2539 article-title: A chemical biology approach identifies AMPK as a modulator of melanoma oncogene MITF publication-title: Oncogene – volume: 98 start-page: 295 year: 1999 end-page: 303 article-title: Stat3 as an oncogene publication-title: Cell – volume: 3 start-page: 654 year: 2010 end-page: 664 article-title: STAT3 upregulates the protein expression and transcriptional activity of beta‐catenin in breast cancer publication-title: Int J Clin Exp Pathol – volume: 50 start-page: 572 year: 2010 end-page: 584 article-title: Conformer generation with OMEGA: algorithm and validation using high quality structures from the Protein Databank and Cambridge Structural Database publication-title: J Chem Inf Model – volume: 28 start-page: 4339 year: 2010 end-page: 4345 article-title: Phase IIB trial of oral Midostaurin (PKC412), the FMS‐like tyrosine kinase 3 receptor (FLT3) and multi‐targeted kinase inhibitor, in patients with acute myeloid leukemia and high‐risk myelodysplastic syndrome with either wild‐type or mutated FLT3 publication-title: J Clin Oncol – volume: 8 start-page: 945 year: 2002 end-page: 954 article-title: Activated STAT signaling in human tumors provides novel molecular targets for therapeutic intervention publication-title: Clin Cancer Res – volume: 35 start-page: 994 year: 1992 end-page: 1001 article-title: Inhibitors of protein kinase C. 2. Substituted bisindolylmaleimides with improved potency and selectivity publication-title: J Med Chem – volume: 7 start-page: 634 year: 2009 end-page: 644 article-title: Role of the protein tyrosine kinase Syk in regulating cell‐cell adhesion and motility in breast cancer cells publication-title: Mol Cancer Res – volume: 406 start-page: 742 year: 2000 end-page: 747 article-title: The Syk tyrosine kinase suppresses malignant growth of human breast cancer cells publication-title: Nature – volume: 490 start-page: 61 year: 2012 end-page: 70 article-title: Comprehensive molecular portraits of human breast tumours publication-title: Nature – volume: 486 start-page: 346 year: 2012 end-page: 352 article-title: The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups publication-title: Nature – volume: 6 start-page: e1001001 year: 2010 article-title: A computational approach to analyze the mechanism of action of the kinase inhibitor bafetinib publication-title: PLoS Comput Biol – volume: 52 start-page: 2919 year: 2012 end-page: 2936 article-title: Conformer generation with OMEGA: learning from the data set and the analysis of failures publication-title: J Chem Inf Model – volume: 10 start-page: R25 year: 2008 article-title: Human breast cancer cell lines contain stem‐like cells that self‐renew, give rise to phenotypically diverse progeny and survive chemotherapy publication-title: Breast Cancer Res – volume: 13 start-page: 2604 year: 1999 end-page: 2616 article-title: Suppression of epithelial apoptosis and delayed mammary gland involution in mice with a conditional knockout of Stat3 publication-title: Genes Dev – volume: 105 start-page: 20870 year: 2008 end-page: 20875 article-title: A large‐scale analysis of tissue‐specific pathology and gene expression of human disease genes and complexes publication-title: Proc Natl Acad Sci USA – volume: 10 start-page: R53 year: 2008 article-title: The CD44+/CD24‐ phenotype is enriched in basal‐like breast tumors publication-title: Breast Cancer Res – ident: e_1_2_8_43_1 doi: 10.1016/j.ccr.2006.10.008 – ident: e_1_2_8_38_1 doi: 10.1038/onc.2009.99 – ident: e_1_2_8_22_1 doi: 10.1186/bcr1982 – ident: e_1_2_8_52_1 doi: 10.1371/journal.pone.0007445 – ident: e_1_2_8_47_1 doi: 10.1200/JCO.2001.19.5.1485 – ident: e_1_2_8_25_1 doi: 10.1038/sj.onc.1204349 – ident: e_1_2_8_26_1 doi: 10.1093/annonc/mds586 – ident: e_1_2_8_35_1 doi: 10.3322/caac.20107 – ident: e_1_2_8_42_1 doi: 10.1093/annonc/mdh052 – ident: e_1_2_8_9_1 doi: 10.1371/journal.pcbi.1001001 – ident: e_1_2_8_28_1 doi: 10.1021/ci100031x – ident: e_1_2_8_10_1 doi: 10.1038/nrclinonc.2010.154 – ident: e_1_2_8_4_1 doi: 10.1016/S0022-2836(77)80200-3 – ident: e_1_2_8_14_1 doi: 10.1158/1078-0432.CCR-08-1155 – volume: 23 start-page: 307 year: 2010 ident: e_1_2_8_51_1 article-title: Aurora‐A gene is frequently amplified in basal‐like breast cancer publication-title: Oncol Rep – volume: 3 start-page: 654 year: 2010 ident: e_1_2_8_2_1 article-title: STAT3 upregulates the protein expression and transcriptional activity of beta‐catenin in breast cancer publication-title: Int J Clin Exp Pathol – ident: e_1_2_8_17_1 doi: 10.1158/1078-0432.CCR-06-3045 – ident: e_1_2_8_46_1 doi: 10.1186/bcr2635 – ident: e_1_2_8_48_1 doi: 10.1038/nchembio.216 – ident: e_1_2_8_49_1 doi: 10.1158/1535-7163.MCT-12-0441-T – ident: e_1_2_8_21_1 doi: 10.1021/ac802720e – ident: e_1_2_8_27_1 doi: 10.1200/JCO.2006.06.5664 – ident: e_1_2_8_3_1 doi: 10.1074/jbc.M409792200 – volume: 8 start-page: 945 year: 2002 ident: e_1_2_8_8_1 article-title: Activated STAT signaling in human tumors provides novel molecular targets for therapeutic intervention publication-title: Clin Cancer Res – ident: e_1_2_8_5_1 doi: 10.1126/science.89.2312.365-a – ident: e_1_2_8_19_1 doi: 10.1158/1078-0432.CCR-12-1611 – ident: e_1_2_8_34_1 doi: 10.1158/2159-8290.CD-11-0348 – ident: e_1_2_8_41_1 doi: 10.1021/ci700052x – ident: e_1_2_8_55_1 doi: 10.1593/neo.91084 – ident: e_1_2_8_31_1 doi: 10.1186/bcr2108 – ident: e_1_2_8_7_1 doi: 10.1016/S0092-8674(00)81959-5 – ident: e_1_2_8_29_1 doi: 10.1021/ci300314k – ident: e_1_2_8_53_1 doi: 10.1038/nature11412 – ident: e_1_2_8_50_1 doi: 10.1016/j.cell.2007.09.007 – ident: e_1_2_8_15_1 doi: 10.1038/nature10983 – ident: e_1_2_8_23_1 doi: 10.1200/JCO.2010.28.9678 – ident: e_1_2_8_32_1 doi: 10.1098/rstb.2011.0008 – ident: e_1_2_8_24_1 doi: 10.1182/blood-2009-08-236471 – ident: e_1_2_8_36_1 doi: 10.1016/j.ajhg.2008.02.013 – ident: e_1_2_8_33_1 doi: 10.1210/en.2002-220224 – ident: e_1_2_8_37_1 doi: 10.1073/pnas.0810772105 – volume: 9 start-page: 594 year: 2003 ident: e_1_2_8_20_1 article-title: Tissue microarray analysis of signal transducers and activators of transcription 3 (Stat3) and phospho‐Stat3 (Tyr705) in node‐negative breast cancer shows nuclear localization is associated with a better prognosis publication-title: Clin Cancer Res – ident: e_1_2_8_44_1 doi: 10.1101/gad.10.19.2462 – ident: e_1_2_8_11_1 doi: 10.1101/gad.13.19.2604 – ident: e_1_2_8_56_1 doi: 10.1158/1541-7786.MCR-08-0371 – ident: e_1_2_8_18_1 doi: 10.1038/nm.2454 – ident: e_1_2_8_40_1 doi: 10.1172/JCI44745 – ident: e_1_2_8_54_1 doi: 10.1016/S0167-5699(99)01574-1 – ident: e_1_2_8_16_1 doi: 10.1021/jm00084a004 – ident: e_1_2_8_39_1 doi: 10.1056/NEJMoa063994 – ident: e_1_2_8_30_1 doi: 10.1158/0008-5472.CAN-08-3441 – ident: e_1_2_8_45_1 doi: 10.1038/35021093 – ident: e_1_2_8_6_1 doi: 10.1038/onc.2013.185 – ident: e_1_2_8_12_1 doi: 10.1002/prca.201100077 – ident: e_1_2_8_13_1 doi: 10.1038/35021086 – reference: 18371930 - Am J Hum Genet. 2008 Apr;82(4):949-58 – reference: 22522925 - Nature. 2012 Jun 21;486(7403):346-52 – reference: 19435916 - Cancer Res. 2009 May 15;69(10):4116-24 – reference: 19421152 - Oncogene. 2009 Jun 18;28(24):2337-47 – reference: 23166150 - Ann Oncol. 2012 Dec;23(12):2997-3006 – reference: 20830236 - Int J Clin Exp Pathol. 2010;3(7):654-64 – reference: 17671126 - Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4429-34 – reference: 23136197 - Clin Cancer Res. 2013 Jan 1;19(1):291-303 – reference: 11230495 - J Clin Oncol. 2001 Mar 1;19(5):1485-92 – reference: 14760128 - Ann Oncol. 2004 Feb;15(2):316-23 – reference: 11948098 - Clin Cancer Res. 2002 Apr;8(4):945-54 – reference: 23082786 - J Chem Inf Model. 2012 Nov 26;52(11):2919-36 – reference: 20019840 - Neoplasia. 2009 Dec;11(12):1318-28 – reference: 875032 - J Mol Biol. 1977 May 25;112(3):535-42 – reference: 22213655 - Proteomics Clin Appl. 2012 Jan;6(1-2):102-16 – reference: 19829710 - PLoS One. 2009;4(10):e7445 – reference: 19435818 - Mol Cancer Res. 2009 May;7(5):634-44 – reference: 17116942 - J Clin Oncol. 2006 Dec 20;24(36):5652-7 – reference: 8843198 - Genes Dev. 1996 Oct 1;10(19):2462-77 – reference: 21727130 - Philos Trans R Soc Lond B Biol Sci. 2011 Aug 12;366(1575):2247-59 – reference: 21124949 - PLoS Comput Biol. 2010;6(11):e1001001 – reference: 23728343 - Oncogene. 2014 May 8;33(19):2531-9 – reference: 1552513 - J Med Chem. 1992 Mar 20;35(6):994-1001 – reference: 10458605 - Cell. 1999 Aug 6;98(3):295-303 – reference: 20813035 - Breast Cancer Res. 2010;12(5):R68 – reference: 21296855 - CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 – reference: 10963601 - Nature. 2000 Aug 17;406(6797):742-7 – reference: 17833344 - Science. 1939 Apr 21;89(2312):365-6 – reference: 22019887 - Nat Med. 2011;17(11):1514-20 – reference: 12193580 - Endocrinology. 2002 Sep;143(9):3641-50 – reference: 10963602 - Nature. 2000 Aug 17;406(6797):747-52 – reference: 17591764 - J Chem Inf Model. 2007 Jul-Aug;47(4):1504-19 – reference: 18559090 - Breast Cancer Res. 2008;10(3):R53 – reference: 17229949 - N Engl J Med. 2007 Jan 18;356(3):217-26 – reference: 19118038 - Clin Cancer Res. 2009 Jan 1;15(1):110-8 – reference: 10689303 - Immunol Today. 2000 Mar;21(3):148-54 – reference: 22915752 - Cancer Discov. 2012 Nov;2(11):1036-47 – reference: 17889643 - Cell. 2007 Sep 21;130(6):986-8 – reference: 20733134 - J Clin Oncol. 2010 Oct 1;28(28):4339-45 – reference: 19331382 - Anal Chem. 2009 May 1;81(9):3440-7 – reference: 20235588 - J Chem Inf Model. 2010 Apr 26;50(4):572-84 – reference: 23000897 - Nature. 2012 Oct 4;490(7418):61-70 – reference: 19690537 - Nat Chem Biol. 2009 Sep;5(9):616-24 – reference: 11420660 - Oncogene. 2001 May 3;20(20):2499-513 – reference: 21633165 - J Clin Invest. 2011 Jul;121(7):2723-35 – reference: 20877296 - Nat Rev Clin Oncol. 2010 Dec;7(12):683-92 – reference: 19965662 - Blood. 2010 Apr 1;115(13):2578-85 – reference: 19104045 - Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20870-5 – reference: 17157791 - Cancer Cell. 2006 Dec;10(6):515-27 – reference: 23012245 - Mol Cancer Ther. 2012 Dec;11(12):2693-703 – reference: 20043089 - Oncol Rep. 2010 Feb;23(2):307-12 – reference: 18366788 - Breast Cancer Res. 2008;10(2):R25 – reference: 12576423 - Clin Cancer Res. 2003 Feb;9(2):594-600 – reference: 10521404 - Genes Dev. 1999 Oct 1;13(19):2604-16 – reference: 15507431 - J Biol Chem. 2004 Dec 31;279(53):55827-32 |
| SSID | ssj0038182 |
| Score | 2.2452545 |
| Snippet | Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple‐negative breast cancer... Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple-negative breast cancer... Abstract Some mutations in cancer cells can be exploited for therapeutic intervention. However, for many cancer subtypes, including triple‐negative breast... |
| SourceID | doaj pubmedcentral hal proquest pubmed crossref wiley springer |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 789 |
| SubjectTerms | Addictions Animals Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Breast cancer Cancer Cancer therapies Cell Differentiation - drug effects Cell Line, Tumor Cell Proliferation - drug effects cell state Cell Survival - drug effects Clinical trials Computer applications Drug Delivery Systems Drug dosages EMBO03 EMBO17 EMBO28 Experiments Female Gene expression Gene Expression Profiling Genetic screening Humans Intracellular Signaling Peptides and Proteins - metabolism Kinases Leukemia Life Sciences Mice Molecular Docking Simulation Molecular Targeted Therapy Mutation Organic chemistry Peptides Protein Interaction Domains and Motifs Protein kinase C Protein-tyrosine kinase Protein-Tyrosine Kinases - metabolism Proteomics Proteomics - methods Selectivity Sequence Analysis, RNA Signal Transduction small‐molecule screen Spleen Stat3 protein STAT3 Transcription Factor - metabolism Staurosporine - analogs & derivatives Staurosporine - pharmacology Studies Syk Kinase Syk protein Transcription Transforming Growth Factor beta - genetics Transforming Growth Factor beta - metabolism Triple Negative Breast Neoplasms - metabolism Tumors Tyrosine Xenograft Model Antitumor Assays |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3LbtQwFLVQpUpsEC2vQKkMQrAhauL4leW0ohohYEMrdWfZjk2RSgbNpJXY8Ql8I1_Cvc4DoqqwYTdKLI9zfO74OHN9LiEvdBBBa1nmKniZc84w5njIrbWwB4qhcE1y-_wgl6f87Zk4-6PUF-aE9fbAPXAHRcVj7Vx0FWu4q5WTuvbCx8LXuowxmW3DmjdupvrfYFyG2OCoKZhgB182DtO4QC1IPluBklE_rCvnmAZ5XWNeT5Wc_i-dq9m0HB3fJXcGHUkX_fh3yK3Q7pLtvrLkt3tkcZIyvKELaim-nKfp5BAFfgHvaLei3Rpfsf_8_qMNn5L5N3WYn95RjzxYb-6T0-M3J0fLfKiWkHusn5Pb6EQDEeiZiFK4UCuL52B9sCq4InCnCqulq4JrChE96IJGWxAL2pfcVlxWD8hWu2rDI0IZIMxAGkYIUC5LaxVgX6kGtk6NrViZkdcjgsYPVuJY0eLC4JYCATcAuBkBz8jLqfnX3kPjpoaHOB1TI7S-TheAEGYghPkXITLyHCZz1sdy8c7gNbRLxEMXV_AEe-NcmyFoNwat77EqroCBPJtuQ7jhNNk2rC43ppQC7Y0qVWXkYU-N6atAPaK7HsuImpFmNpb5nfbzebL0BtGqpSwy8mqk1-9h3QBVntj3d0DN-4-H_afH_wPaJ-Q29Cz6pPU9stWtL8NT0GSd20_h9wv6uTHy priority: 102 providerName: Directory of Open Access Journals – databaseName: Health & Medical Collection dbid: 7X7 link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3ba9YwFA86EXwR76tOiSL6Ylnb3NqnsYnjQ9QXN_jeQpImm-Da-bUT9t_vnPQyytjeSpu2ybn0_JKe_A4hH0svfFnKPFXeyZTzAn2O-9QYA3Og4DNbR7bPX3J1zL-vxXpccOvGtMrpmxg_1HXrcI18F3nJsWSp4Hvn_1KsGoV_V8cSGvfJA6Quw5QutZ4nXBiMipFXUxSi2D3rLCZzAWaQfBGHIl0_RJdTTIa8iTRvJkzOf02XmDYGpcMn5PGIJun-oP6n5J5vnpGHQ33Jy-dk7yjmecMjqKG4RE_j_iEKI4bh0L6l_QYX2tPGn0QCcGoxR72nDm1h070gx4ffjr6u0rFiQuqwhk5qghU1eKErRJDC-koZ3AvrvFHeZp5blZlSWuZtnYngABvUpQHAULqcG8Yle0m2mrbx24QWlYPIzqoATsplbowqas5UDdOn2rAiT8iXSX7ajXTiWNXir8ZpBYpbg7j1JO6EfJqbnw88Grc1PEBlzI2Q_jqeaDcnevQmnTEeKmuDZdApWykrS-iuC5mryjwEmZAPoMrFM1b7PzSeQ8pE3HjxH0awM2laj47b6WszS8j7-TK4HCrJNL696HQuBVIcMcUS8mowjPlVgCCRYa9IiFqYzKIvyyvNn9NI6w3AtZQyS8jnybiuu3WLqNJoe3cLVP_8fTAcvb57wG_II7hHDCnpO2Sr31z4t4C4evsuutUVFKcmrA priority: 102 providerName: ProQuest – databaseName: Springer Nature OA Free Journals dbid: C6C link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1Lb9QwELagCIlLxZtAQQYhuBCRxM8ctyuqFQIutFJvlu3YFAmy1W6KxI2fwG_klzDjPCBaFXGLHMeZzCMztsffEPJcBxG0lmWugpc55xXaHA-5tRbmQDEUrklonx_k6oS_PRWnQxINnoX5e_9eVKJ6_XXrMAEL_LzkV8k1UTKJyruUy_GHiz6nGuAzdx6ZuZuEyg9O5AxzHncDyt28yGlzdB66Jt9zdJPsD0EjXfRSvkWuhPY2ud6Xkfx-hyyOUzo3DEEtxZV4mo4JUVAmUDLarWm3wfX0Xz9-tuFTQvqmDpPRO-pR6JvtXXJy9OZ4ucqH0gi5x2I5uY1ONGBuvhJRChdqZfHQqw9WBVcE7lRhtXQsuKYQ0UMQ0GgLkYH2JbeMS3aP7LXrNjwgtKo9uHBWR7BGLktrVdVwphqYJzWWVWVGXo0cNH7ADcfyFV8Mzh-Q4QYYbkaGZ-TF1P28B8y4rOMhimPqhDjXqQHEbwazMQXjsXYuOgZEuVo5qYFcHwtf6zJGmZFnIMzZGKvFO4NtiI2IJyy-wRccjLI2g4VuDeLcYwlcAYQ8nW6DbaGYbBvWF1tTSoFYRkyxjNzvVWN6FYSKCKVXZUTNlGZGy_xO-_ks4XdDhKqlLDLyclSvP2Rdwqo8ad-_GWrefzzsrx7-98iPyA24FH0a-gHZ6zYX4TFEWZ17kmzsN0bOH9I priority: 102 providerName: Springer Nature – databaseName: Wiley Online Library Open Access dbid: 24P link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1bi9UwEA66Ivgi3q2uEkX0xWLbXPt4VlwOoiK4C_sWkjTZXdAeOe0KvvkT_I3-EmfSi5ZlBd9KmqaTyUxnks58Q8gzHUTQWpa5Cl7mnFeoczzk1lrYA8VQuCahfX6Q60P-9kgcjXVOMRdmwIeYD9xQM9L3GhXcum6q2IOooV86h6FZ4AFIfplcwfRaBM-v-MfpU4zWqBoyInmOdZlGkE0c4NXfjy-MUsLuB1NzgpGR593O89GT8y_UpYObLNT-DXJ9dC3papCFm-RSaG-Rq0Oxye-3yeogBX3DENRSPK-nKZmIwrxBFGm_of0WT91__fjZhuOEB04dhqz31KNobLs75HD_zcHrdT4WUMg9ltTJbXSiAaX0lYhSuFAri6mxPlgVXBG4U4XV0rHgmkJED65Coy34D9qX3DIu2V2y027acJ_QqvZg6FkdQWe5LK1VVcOZamA31VhWlRl5OXHQ-BFdHItcfDa4y0CGG2C4mRiekedz968DrMZFHfdwOeZOiIadGjbbYzMqlykYj7Vz0TEgytXKSQ3k-lj4Wpcxyow8hcVcjLFevTPYhgiKmIfxDWawO621GfW4M4iGj4VyBRDyZL4NGojLZNuwOetMKQUiHjHFMnJvEI35VeBQIuBelRG1EJoFLcs77elJQvkGP1ZLWWTkxSRef8i6gFV5kr5_M9S8_7Q3XD34z_4PyTVoFEPI-i7Z6bdn4RF4ZL17nLTuN2lMLFc priority: 102 providerName: Wiley-Blackwell |
| Title | Targeting a cell state common to triple‐negative breast cancers |
| URI | https://link.springer.com/article/10.15252/msb.20145664 https://onlinelibrary.wiley.com/doi/abs/10.15252%2Fmsb.20145664 https://www.ncbi.nlm.nih.gov/pubmed/25699542 https://www.proquest.com/docview/2290195054 https://www.proquest.com/docview/1657328373 https://hal.umontpellier.fr/hal-02276743 https://pubmed.ncbi.nlm.nih.gov/PMC4358660 https://doaj.org/article/034f9bbfb32d4b97b689c5cf0c981ff6 |
| Volume | 11 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1fb9MwELfYJiReEP8JjMogBC8E8sexkweE2mpThdg0wSr1zbIde0MaKaQZYm98BD4jn4Q7J80UlSFeqjRxk-vd73Rn5_w7Qp7nNrN5zuNQWMNDxhL0OWZDpRTMgZyNdOnZPg_5bM7eL7LFJaVQp8DVX6d22E9qXp-9_vHt4h04_Nuue0_y5stKY5EW5AKcbZEdCEoCffSA9S8UMC4l7d5IFmKHpo5uc-Png_DkWfwh6JxijeRmArpZR9m_TB2muj5W7d8iN7skk45bVNwm12x1h1xv205e3CXjY1_-DbegiuLKPfXbiiiAD0BJmyVtalx___3zV2VPPDM41Vi83lCDIKlX98h8f-94Ogu7VgqhweY6oXI6K8E9TZI5nmlbCIWbZI1VwurIMi0ilXOdWl1GmTOQNJS5gkwiNzFTKePpfbJdLSv7kNCkMBDy08KB9zIeKyWSkqWihHlVqdIkDsirtQal6XjGsd3FmcT5BipcgsLlWuEBedEP_9oSbFw1cILm6AchL7Y_saxPZOdmMkqZK7R2OgWhdCE0z0Fc4yJT5LFzPCDPwJiDe8zGHySeQy5F3JHxHf7B7trWcg1Iibz42DI3A0Ge9pfBF9FMqrLL85WMeYbcR6lIA_KghUb_KEgtkXovCYgYgGYgy_BK9fnU831DRptzHgXk5Rpel2JdoarQo-_fCpUHnybt0aP_tcFjcgMOs7ZqfZdsN_W5fQJJWaNHZCthR_ApFmJEdiZ7h0cf4duUT0d-mWPk3fEPioc07w |
| linkProvider | Scholars Portal |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9QwEB6VrRBcEG8CBQzicWnUPGwnOaCqC622dLtCsJV6M7bjtEiQlN0tqH-K38hMHltFVXvrbZU4XmfeE4-_AXiTOuHSVIZ-4qz0OY9I57jztdaYAxUuMHmN9jmRowP--VAcrsC_7iwMlVV2NrE21Hll6Rv5BuGSU8tSwTdPfvvUNYp2V7sWGo1Y7Lmzv5iyzT_sfkL-vo2ine3px5HfdhXwLfWZ8XVhRI6SaiNRSGFclmg6L2qdTpwJHDdJoFNpYmfyQBQW_WeeanSqqQ25jrmMcd4bsMpjTGUGsDrcnnz52tl-cn9Ri-QpIhFt_JobKh_DKEXynuerGwSgPzum8suLse3FEs3lPm0_iq7d4M5duNPGr2yrEbh7sOLK-3Cz6Wh59gA2p3VlOU7BNKNNAVafWGJIYyQgW1RsMaNP-37pjmrIcWaoKn7BLEnfbP4QDq6Fmo9gUFalewIsyizGEnFWoFngMtQ6iXIeJzkmbLmOo9CD9Y5-yrYA5tRH46eiRIbIrZDcqiO3B--Ww08a5I7LBg6JGctBBLhdX6hmR6rVXxXEvMiMKUyMizJZYmSKy7VFYLM0LArpwWtkZW-O0dZY0TUCaaSjHn_wDdY6TqvWVMzVuWB78Gp5G5WcmKRLV53OVSgFgSrFSezB40Ywln-FMSth-kUeJD2R6a2lf6f8cVwDiWOonEoZePC-E67zZV1CKr-WvasJqva_DZtfT69-4ZdwazTdH6vx7mTvGdzG50VTEL8Gg8Xs1D3HeG9hXrRKxuD7dev1fyDNZSU |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3NbtQwELZKKxAXxD-BAgYhuBA1iR3HEacUWC1LqZDaSr1ZtmO3SG222k2RuPEIPCNPwoyTLIpWRdwix3Em85MZJzPfEPJKutxJKdK4cFbEnGdoc9zFWmvYA3mXmDqgfe6L6RGfHefHG-TdUAsTst2HX5JdTQOiNDXtzkXth3492c750mBaFnh_wa-RLSkSCTuvraqaHcyGFzH6oqyH1Vy7aOSGAlo_OJdTzIVcDzTX8yVXP03HIW3wSZPb5FYfTNKqk_4dsuGau-R6117yxz1SHYY0b1iCaopf6GkoH6LwvKB8tJ3TdoHf2X___NW4k4AATg0mqbfUojIslvfJ0eTj4ftp3LdMiC020Ym1N3kNZmiz3IvcuLLQWAxrnS6cSRw3RaKlMMyZOsm9heCglhoiBmlTrhkX7AHZbOaNe0RoVlpw7az0YKVcpFoXWc1ZUcP-qdYsSyPyduCgsj2eOLa1OFO4r0CGK2C4Ghgekder6RcdkMZVE3dRHKtJiH8dBuaLE9Wbk0oY96Ux3jAgypSFERLItT6xpUy9FxF5CcIcrTGt9hSOIWYiVl58hyfYHmStestdKsS_x9a4ORDyYnUabA7FpBs3v1yqVOSIccQKFpGHnWqsbgUhJELsZREpRkozomV8pvl2GnC9IXKVQiQReTOo11-yrmBVHLTv3wxVXw52u6PH_73yc3Lj64eJ2vu0__kJuQmjeZepvk0228WlewqBWGue9Qb3B7boLG0 |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Targeting+a+cell+state+common+to+triple%E2%80%90negative+breast+cancers&rft.jtitle=Molecular+systems+biology&rft.au=Muellner%2C+Markus+K&rft.au=Mair%2C+Barbara&rft.au=Ibrahim%2C+Yasir&rft.au=Kerzendorfer%2C+Claudia&rft.date=2015-02-01&rft.issn=1744-4292&rft.eissn=1744-4292&rft.volume=11&rft.issue=2&rft_id=info:doi/10.15252%2Fmsb.20145664&rft.externalDBID=n%2Fa&rft.externalDocID=10_15252_msb_20145664 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1744-4292&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1744-4292&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1744-4292&client=summon |